The ability of a human artery to pass through 150 million liters of blood sustaining 2 billion pulsations of blood pressure with
minor deterioration depends on unique construction of the arterial wall. Viscoelastic properties of this construction enable to re-seal the
occuring damages apparently without direct immediate participance of the constituent cells. Collagen structures are considered to be the
elements that determine the mechanoelastic properties of the wall in parallel with elastin responsible for elasticity and resilience. Collagen
scaffold architecture is the function-dependent dynamic arrangement of a dozen different collagen types composing three distinct interacting
forms inside the extracellular matrix of the wall.
Tightly packed molecules of collagen types I, III, V provide high tensile strength along collagen fibrils but toughness of the collagen
scaffold as a whole depends on molecular bonds between distinct fibrils. Apart of other macromolecules in the extracellular matrix
(ECM), collagen-specific interlinks involve microfilaments of collagen type VI, meshwork-organized collagen type VIII, and FACIT collagen
type XIV. Basement membrane collagen types IV, XV, XVIII and cell-associated collagen XIII enable transmission of mechanical
signals between cells and whole artery matrix.
Collagen scaffold undergoes continuous remodeling by decomposition promoted with MMPs and reconstitution from newly produced
collagen molecules. Pulsatile stress-strain load modulates both collagen synthesis and MMP-dependent collagen degradation. In this way
the ECM structure becomes adoptive to mechanical challenges.
The mechanoelastic properties of the arterial wall are changed in atherosclerosis concomitantly with collagen turnover both type-specific
and dependent on the structure. Improving the feedback could be another approach to restore sufficient blood circulation.